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Na(v)1.7 and Na(v)1.8: Role in the pathophysiology of pain
Chronic pain is a significant unmet medical problem. Current research regarding sodium channel function in pathological pain is advancing with the hope that it will enable the development of isoform-specific sodium channel blockers, a promising treatment for chronic pain. Before advancements in the...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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SAGE Publications
2019
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6589956/ https://www.ncbi.nlm.nih.gov/pubmed/31172839 http://dx.doi.org/10.1177/1744806919858801 |
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author | Hameed, Shaila |
author_facet | Hameed, Shaila |
author_sort | Hameed, Shaila |
collection | PubMed |
description | Chronic pain is a significant unmet medical problem. Current research regarding sodium channel function in pathological pain is advancing with the hope that it will enable the development of isoform-specific sodium channel blockers, a promising treatment for chronic pain. Before advancements in the pharmacological field, an elucidation of the roles of Na(v)1.7 and Na(v)1.8 in the pathophysiology of pain states is required. Thus, the aim of this report is to present what is currently known about the contributions of these sodium channel subtypes in the pathophysiology of neuropathic and inflammatory pain. The electrophysiological properties and localisation of sodium channel isoforms is discussed. Research concerning the genetic links of Na(v)1.7 and Na(v)1.8 in acquired neuropathic and inflammatory pain states from the scientific literature in this field is reported. The role of Na(v)1.7 and Na(v)1.8 in the generation and maintenance of abnormal neuronal electrogenesis and hyperexcitability highlights the importance of these channels in the development of pathological pain. However, further research in this area is required to fully elucidate the roles of Na(v)1.7 and Na(v)1.8 in the pathophysiology of pain for the development of subtype-specific sodium channel blockers. |
format | Online Article Text |
id | pubmed-6589956 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-65899562019-06-28 Na(v)1.7 and Na(v)1.8: Role in the pathophysiology of pain Hameed, Shaila Mol Pain Review Chronic pain is a significant unmet medical problem. Current research regarding sodium channel function in pathological pain is advancing with the hope that it will enable the development of isoform-specific sodium channel blockers, a promising treatment for chronic pain. Before advancements in the pharmacological field, an elucidation of the roles of Na(v)1.7 and Na(v)1.8 in the pathophysiology of pain states is required. Thus, the aim of this report is to present what is currently known about the contributions of these sodium channel subtypes in the pathophysiology of neuropathic and inflammatory pain. The electrophysiological properties and localisation of sodium channel isoforms is discussed. Research concerning the genetic links of Na(v)1.7 and Na(v)1.8 in acquired neuropathic and inflammatory pain states from the scientific literature in this field is reported. The role of Na(v)1.7 and Na(v)1.8 in the generation and maintenance of abnormal neuronal electrogenesis and hyperexcitability highlights the importance of these channels in the development of pathological pain. However, further research in this area is required to fully elucidate the roles of Na(v)1.7 and Na(v)1.8 in the pathophysiology of pain for the development of subtype-specific sodium channel blockers. SAGE Publications 2019-06-21 /pmc/articles/PMC6589956/ /pubmed/31172839 http://dx.doi.org/10.1177/1744806919858801 Text en © The Author(s) 2019 http://creativecommons.org/licenses/by-nc/4.0/ Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Review Hameed, Shaila Na(v)1.7 and Na(v)1.8: Role in the pathophysiology of pain |
title | Na(v)1.7 and Na(v)1.8: Role in the pathophysiology of pain |
title_full | Na(v)1.7 and Na(v)1.8: Role in the pathophysiology of pain |
title_fullStr | Na(v)1.7 and Na(v)1.8: Role in the pathophysiology of pain |
title_full_unstemmed | Na(v)1.7 and Na(v)1.8: Role in the pathophysiology of pain |
title_short | Na(v)1.7 and Na(v)1.8: Role in the pathophysiology of pain |
title_sort | na(v)1.7 and na(v)1.8: role in the pathophysiology of pain |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6589956/ https://www.ncbi.nlm.nih.gov/pubmed/31172839 http://dx.doi.org/10.1177/1744806919858801 |
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